IHD Patho Flashcards
Myocardial Ischemia
Lack of oxygen and reduced blood flow to the myocardium resulting in an imbalance between myocardial oxygen supply and demand
Myocardial Infarction
Necrosis (death) of heart muscle caused by an imbalance between oxygen supply and demand
Angina Pectoris
“Chest pain”; pain or discomfort in the chest or adjacent areas which is due to myocardial ischemia
Silent Ischemia
Painless episodes of myocardial ischemia (75% of all ischemia)
Silent Infarction
Infarction occurring without chest pain or other common symptoms of ischemia; about 20% of all first infarcts
Acute Coronary Syndrome
Unstable angina or acute myocardial infarction
Myocardial Oxygen Demand
- Heart Rate
- Wall Tension
- Contactility
Wall Tension
- Related to ventricular volume and wall pressure
- Preload v.s. Afterload
Myocardial Oxygen Supply
- Coronary Blood Flow
- Collaterals
- Autoregulation
- Other factors that regulate coronary blood flow
Coronary Blood Flor
- Increased oxygen demand must be met by an increase in coronary blood flow
- Coronary blood flow can normally increase 5x resting value
- Coronary blood flow occurs primarily during diastole
- May be altered by fixed obstruction or vasospasm
Collaterals
- Provide blood flow when major vessels are obstructed
- Development enhanced by gradual coronary occlusion, exercise, severe anemia
- May prevent a myocardial infarction in the presence of total occlusion
Autoregulation
-As larger coronary arteries become occluded or stenotic, smaller vessels dilate to maintain coronary blood flow
Other Factors
- Neural (symp v.s. parasymp.)
- Endothelium - EDRF, endothelin, prostaglandins, others
- Metabolic - oxygen, carbon dioxide, adenosine
Oxygen Extraction
- At rest, 65-75% of oxygen passing through myocardium is extracted
- With increased oxygen demand, oxygen extraction can approach 80%
Blood Oxygen Content
- Hemoglobin/hematocrit
- Arterial blood gases
Types of Ischemic Heart Disease
- Chronic Stable Angina
- Unstable Angina
- Vasospastic Angina (Prinzmetal’s Variant)
- Myocardial Infarction (MI)
Chronic Stable Angina
- Associated with a certain level of physical activity or emotional stress
- Relieved by rest or nitroglycerin
Unstable Angina
- Angina of new onset, usually within one month and brought on by minial exertion
- Development of crescendo (more severe) pain superimposed on preexisting exertion-related angina
- Any change in angina frequency, intensity, or duration
- Pain at rest
- No elevated cardiac enzymes or ST-segment elevation
Vasospastic Angina
- Occurs in patients with or without coronary heart disease and is due to a spasm of a coronary artery that decreases myocardial blood flow
- More likely to experience pain at rest and in the early morning hours
- Pain not usually brought on by exertion or emotional stress or relieved by rest
- Occurs more often in smokers, young patients, with illicit drug use, and with alcohol withdrawal
Myocardial Infarction
- Most common due to artherosclerotic thrombosis
- Coronary spasm and coronary embolus may also cause infarction
- ST-segment and Non-ST segment elevation MI
STEMI
- ST-segment elevation MI
- MI characterized by ST-segment elevation on the ECG in at least 2 contiguous leads of >= 2 mm in men or >= 1.5 mm in women in leads V2-V3 and/or ?= 1 mm in other contiguous chest leads or the limb leads
- More extensive infarct
- Higher hospital mortality rate
- Elevated cardiac enzymes
NSTEMI
- Non-ST-segment elevation MI
- Damage to myocardium is not as extensive
- Increased likelihood of developing post-infarction angina and early reinfarction
- Elevated cardiac enzymes
Type I MI
- Spontaneous MI
- Due to atherosclerotic plaque rupture and thrombus formation
- Vast majority of MI
Type II MI
- Due to ischemic imbalance
- NOT due to plaque rupture, but end result is in inadequate oxygenation of myocardial tissue
- EX: coronary vasospasm, hypotension, anemia, etc.
Type 3 MI
- Fatal MI in the setting of no cardiac biomarkers
- REsults in death and suspected based on symptoms and ECG findings
- No cardiac biomarkers obtained
Type 4a MI
- Due to PCI
- Confirmed by troponin elevations and one or more of the following:
1. Symptoms of ischemia
2. ECG changes
3. Angiographic evidence of coronary artery obstruction
4. Imaging evidence of myocardial damage
Type 4b MI
- Due to stent thrombosis
- Confirmed by an increase in cardiac biomarkers
Type 5 MI
- Due to CABG
- Confirmed by the increase in cardiac biomarkers and one or more of the following:
1. New Q waves or left bundle branch block on ECG
2. Angiographic evidence of new coronary artery obstruction
3. Imaging evidence of myocardial damage
Patho of Atherosclerosis
- Phase 1: small plaque that is present in most people < 30 y.o., usually progresses slowly
- Phase 2: Plaque, not necessarily stenotic, with high lipid content and is prone to rupture
- Phase 3: Plaque rupture with mural thombosis formation, leads to an increase in artery stenosis and possibly angina
- Phase 4: Plaque rupture leading to an acute coronary occlusion, leads to unstable angina, AMI, or ischemic sudden death
- Phase 5: Severely stenotic or occlusion plaques organized by connective tissue, may become complicated by a thrombus and/or myoproliferative response leading to an acute silent occlusive process
Plaque Rupture
- Most complications of atherosclerosis are due to plaque rupture
- Rupture tends to occur at junctions, branches, or bends in the vessel
Clot Formation
- Platelet deposition: first step in hemostasis and thrombus formation, increases with an increase in shear force
- Platelet activation causes conformational change in GP IIb/IIIa receptor, allowing it to bind to fibrinogen
- Fibrinogen cross-links develop and form bridges to otehr platelets, facilitating aggregation and ultimately platelet plug
- Platelets generate thrombin and convert fibrinogen to fibrin which converts white thrombus to a stable red-thrombus
- Plaque composition may be MOST important determinant for plaque rupture/fissure
Glycoproteins
- Different GP adhere to various adhesive proteins found in subendothelial matrix which are exposed by vessel damage
- GP Ib: binds von Willebrand factor
- GP Ia/IIA: binds collagen
- GP Ic/IIa: binds fibronectin
- GP IIb/IIa: plays a secondary role in platelet adhesion
History/Risk Factor Assessment
- Part of Diagnosis of IHD
- No physical findings are specific for angina
- Characteristics of pain
- Laboratory assessment is not helpful except for cardiac enzymes
- Patient’s cardiac risk factors
- Pain with unstable angina typically lasts 10-20 minutes
- Pain with non-ST-elevation MI typically lasts up to an hour
- Pain with an ST-elevation MI typically lasts > 1 hour
ECG
- Used in diagnosis of IHD
- Resting ECG is normal in about 30-50% of patients with angina
- ST-T wave changes
- Q waves with infarction
- Use of ambulatory monitoring to detect silent ischemia
Exercise Tolerance Testing (ETT)
- Used in diagnosis of IHD
- Useful for assessing the severity and prognosis of CAD
- Positive test indicated by angina, ECG changes, or dysrhythmias
- Abnormal BP or HR response may signal CAD
Radionuclide Imaging
- Used in diagnosis of IHD
- Patient is stressed with either exercise or pharmacologically and then myocardial imaging performed using either sestamibi or thallium
- Defect in myocardial uptake of sestamibi or thallium indicates ischemia or infarction
- More expensive than ETT
Radionuclide Imaging Useful for patients….
- Unable to exercise completely
- Asymptomatic with abnormal results on ETT
- Men with typical angina who have “negative” results on ETT
- Women with typical angina who have equivocal ETT results
- Patients with known CAD to determine myocardial viability
Coronary Angiography
- Used in diagnosis of IHD and definitive diagnosis of CAD
- Allows determination of location and extent of atherosclerosis
- Used when bypass surgery or angioplasty are being contemplated for therapy
- Does not give functional information
Cardiac Enzymes
- Used in diagnosis of IHD
- Creatine kinase (CK or CPK)
- Isoenzymes: MM (muscle), BB (brain), MB (myocardium)
- Troponins I and T